1985 Fiscal Year Final Research Report Summary
Etiopathogenesis of Immunological Diseases: Cell Sociological aspect of tissue-destructive mechanisms on them
| Project/Area Number |
59440029
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Human pathology
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| Research Institution | Tohoku University |
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Principal Investigator |
NOSE Masato 東北大学, 医, 講師 (70030913)
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| Project Period (FY) |
1984 – 1985
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| Keywords | glomerulonephritis / angitis / granuloma / monoclonal antibody / immunocomplex / retrovirus / macrophage / リンホカイン |
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| Research Abstract |
Intractable inflammatory diseases occupying almost all of "Collagen Diseases" seem to be somehow under immunological disturbance. The etiopathogenesis of such diseases may be much complicated as the primary feature of disease is completely hidden by secondary or tertiary host reactions. Recent advances in immunology make it possible to explain the mechanisms on primary disorders or afferent arms of these diseases, but the efferent arms in tissue-destructive mechanisms as found in granulomas are still obscure. We tired to clarify the latter on the basis of "cell sociology among cell to cell interactions of assailants, sufferers and hecklers" as follows.
A. The basic pathological feature in immunological diseases; glomerulonephritis, angitis and glanulomas were analyzed in immunohistochemical studies using monoclonal antibodies against various cell surface antigens.
B. Some host causes for development and progression of the diseases were eluted and four of them were studied in new approachs and new methods;
(1) immune complexes:
molecular manipulations of IgG to analyze their effector functions,
(2) retroviruses :
immunopathological and virological analysis of their roles in immunocytolysis,
(3) macrophages :
significant roles of their functional abnormalities in the development of granulomatous lesions, and roles of regulatory cytokines to macrophages, and
(4) T cell products :
significance as inhibitors but sometimes accelerators against intractable inflammatory lesions.
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Research Products
(10 results)
